ArticleClinical and experimental immunology2005
Induction of proinflammatory mediators requires activation of the TRAF, NIK, IKK and NF-kappaB signal transduction pathway in astrocytes infected with Escherichia coli.
Article in Clinical and experimental immunology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 41 citations in OpenAlex.
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- Rosuvastatin Reduces Neuroinflammation in the Hemorrhagic Transformation After rt-PA Treatment in a Mouse Model of Experimental Stroke.Frontiers in cellular neuroscience · 2018Article
- Rac1 regulates bacterial toxin-induced thrombin generation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016Article
- Astrocytes Are Primed by Chronic Neurodegeneration to Produce Exaggerated Chemokine and Cell Infiltration Responses to Acute Stimulation with the Cytokines IL-1β and TNF-α.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Rac1 regulates platelet shedding of CD40L in abdominal sepsis.Laboratory investigation; a journal of technical methods and pathology · 2014Article
- Rho kinase regulates induction of T-cell immune dysfunction in abdominal sepsis.Infection and immunity · 2013Article
- Ursodeoxycholic acid but not tauroursodeoxycholic acid inhibits proliferation and differentiation of human subcutaneous adipocytes.PloS one · 2013Article
- Brain-derived neurotrophic factor induces proliferation of human airway smooth muscle cells.Journal of cellular and molecular medicine · 2012Article
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- RNAi screen in mouse astrocytes identifies phosphatases that regulate NF-kappaB signaling.Molecular cell · 2006Article
- The glia-neutrophil axis: an understudied crosstalk in bacteria-induced neuroinflammation.Frontiers in neurologyReview
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Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Escherichia coli is associated with inflammation in the brain. To investigate whether astrocytes are involved in E. coil-induced inflammation, we assessed the levels of expression of proinflammatory mediators produced by E. coli-infected astrocytes. E. coli infection in primary human astrocytes and cell lines increased expression of the CXC chemokine IL-8/GRO-alpha, the CC chemokine MCP-1, TNF-alpha, and iNOS. E. coli infection activated p65/p50 heterodimeric NF-kappaB and concurrently decreased the signals of IkappaBalpha. Blocking the NF-kappaB signals by IkappaBalpha-superrepressor-containing retrovirus or antisense p50 oligonucleotide transfection resulted in down-regulation of expression of the proinflammatory mediators. Furthermore, superrepressors of IkappaBalpha, IkappaB kinase (IKK) or NF-kappaB inducing kinase (NIK) inhibited the up-regulated expression of the downstream target genes of NF-kappaB such as IL-8 and MCP-1, and superrepressors of TNF receptor-associated factor (TRAF)2 and TRAF5 also inhibited expression of the E. coli-induced target genes of NF-kappaB. These results indicate that proinflammatory mediators such as the CXC chemokine IL-8/GRO-alpha, the CC chemokine MCP-1, TNF-alpha, and iNOS can be expressed in E. coli-infected astrocytes via an NF-kappaB pathway, suggesting that these mediators may contribute to inflammation in the brain, including infiltration of inflammatory cells.
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